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PubMed1985

Clearance of triglycerides from the circulation and its relationship to serum lipoproteins: influence of age and sex.

In this study of a randomly selected population from 20 to 70 years of age, the clearance of triglycerides from the blood was studied after i.v. injection of an artificial triglyceride emulsion Intralipid. In women, the triglyceride clearance from the blood decreases with increasing age, but for men there was no change with age. Women had faster fractional removal rates of i.v. injected triglycerides than men in all age-groups. The triglyceride clearance showed a negative correlation to Broca index (obesity), serum triglyceride, serum cholesterol, triglycerides in very low density lipoproteins, and to cholesterol in very low density lipoproteins and in low density lipoproteins, but showed a strong positive correlation to cholesterol in high density lipoproteins.

Adult↗
PubMed1988

Effects of dietary casein and soybean protein on triglyceride turnover in rat liver.

We previously found that hepatic lipogenic enzyme induction, fatty acid synthesis, and triglyceride level were markedly lower in rats fed soybean protein than in those fed casein (Iritani et al. (1986): J. Nutr., 116: 190). After labeling triglycerides with tritiated water, the effects of dietary protein on the triglyceride degradation have been investigated. After the injection of tritiated water into rats, the radioactivities of fatty acids and triglycerides reached a plateau in 1-2 days and were markedly lower in the soybean protein group than in the casein group. The decreasing rates of triglyceride radioactivities were similar between the casein and soybean protein groups. The enzyme activities in glycerolipid synthesis were similar between the groups. Therefore, the lowering effects of soybean protein on triglyceride levels appear to be ascribed to triglyceride synthesis (due to fatty acid synthesis) rather than to the degradation.

Animals↗
PubMed1999

Olanzapine increases weight and serum triglyceride levels.

BACKGROUND: Previous studies have suggested that clozapine is associated with increases in both weight and serum triglyceride (but not cholesterol) levels. Because of the pharmacologic similarities between clozapine and olanzapine, we decided to evaluate if olanzapine use was associated with an increase in triglycerides. METHOD: Twenty-five inpatients (21 men, 4 women) were treated with olanzapine, and their outcomes were tracked prospectively in a medication utilization evaluation study. RESULTS: After 12 weeks on a mean +/- SD dose of 13.8+/-4.4 mg/day, weight increased a mean of 12 lb (5.4 kg; from 190+/-37 lb [85.5+/-16.7 kg] to 202+/-30 lb [90.9+/-13.5 kg]), while fasting triglycerides increased a mean of 60 mg/dL (from 162+/-121 mg/dL to 222+/-135 mg/dL). Both increases were significant at p < .05. Fasting total cholesterol did not increase. The triglyceride increase was even larger when we excluded 8 patients who received various interventions to lower lipid levels (e.g., pravastatin, low-fat diet) during the olanzapine trial. There was a strong association between weight change and triglyceride change (p < .02); after controlling for weight, analysis of covariance showed no independent increase in triglycerides. CONCLUSION: These results suggest olanzapine has significant effects on weight and serum triglyceride levels. Clinical implications are discussed.

Adult↗
PubMed2001

A lipogenic diet in mice with a disruption of the stearoyl-CoA desaturase 1 gene reveals a stringent requirement of endogenous monounsaturated fatty acids for triglyceride synthesis.

Stearoyl-CoA desaturase (SCD) catalyzes the de novo biosynthesis of oleate and palmitoleate, which are the major fatty acids found in triglycerides, cholesteryl esters, and phospholipids. A high carbohydrate (lipogenic) diet induces lipogenic gene expression by sterol regulatory element binding protein 1 (SREBP-1c)-mediated gene transcription, leading to an increase in the synthesis of triglycerides. The lipogenic diet fed to mice with a null mutation in the SCD1 gene (SCD-/-) fails to induce the synthesis of triglycerides in liver, despite the induction of expression of SREBP-1 and its target genes, fatty acid synthase and glycerol-3-phosphate acyltransferase. The lipogenic diet led to a decrease in the levels of triglyceride, but an increase in the level of cholesteryl esters of saturated fatty acids. Feeding a lipogenic diet supplemented with high levels of oleate to the SCD-/- mice resulted in incorporation of oleate in the liver of SCD-/- mice, but failed to restore triglycerides to the levels in the normal mouse. Triglyceride synthesis, as measured by the incorporation of [(3)H]glycerol, was dramatically reduced in the liver of SCD-/- mouse fed a lipogenic diet compared with the normal mouse. These observations demonstrate that induction of triglyceride synthesis is highly dependent on SCD1 gene expression.

Animals↗
PubMed2002

[The relationship between insulin resistance and postprandial abnormal serum triglyceride metabolism in essential hypertension].

OBJECTIVE: To investigate the relationship between insulin resistance (IR) and postprandial abnormal metabolism of serum triglyceride-rich lipoprotein in essential hypertension (EH). METHODS: In 44 patients with EH and 22 normal subjects (NS). Total cholesterol, HDL cholesterol, LDL cholesterol, apoliprotein AI and apoliprotein B in fasting serum and serum triglyceride before and 2, 4, 6, 8 hours after a standardized fat loading were measured. Triglyceride peak response (TGPR) and the area under triglyceride curve (TG-AUC) over 8 hours were taken as the index of abnormal TG metabolism. Standardized 75 g oral glucose tolerance test was carried, the area under insulin curve (IS-AUC) over 3 hours and insulin sensitivity index were taken as the index of insulin sensitivity. RESULTS: TGPR and TG-AUC were higher in EH than those in NS (TGRP: 4.14 mmol/L +/- 3.0 mmol/L vs 2.06 mmol/L +/- 1.32 mmol/L, P < 0.01; TG-AUC: 20 mmol/L +/- 6 mmol/L vs 10 mmol/L +/- 4 mmol/L, P < 0.05). 65.9% of EH had postprandial abnormal serum triglyceride metabolism. IS-AUC was higher in EH than that in NS, and ISI was lower in EH than that in NS. The incidence of IR in EH was 61%. 44 EH were categorized into 2 groups according to insulin sensitivity: EH with IR (n = 27) and EH with normal insulin sensitivity (NIS, n = 17). TGPR and TG-AUC in EH with IR were significantly higher than those in EH with NIS (TGPR: 5.25 mmol/L +/- 3.03 mmol/L vs 3.16 mmol/L +/- 1.46 mmol/L, P < 0.05; TG-AUC: 25 +/- 13 mmol/L vs 13 +/- 7 mmol/L, P < 0.01). No significant difference was found between EH with NIS and NS (P > 0.05). TG-AUC and TRPG was positively related to IS-AUC and negatively related to ISI. CONCLUSION: Patients with EH had postprandial abnormal serum triglyceride metabolism, insulin resistance may aggravate postprandial triglyceride metabolism in EH.

Adult↗
PubMed1992

Accumulation and mobilization of triglycerides and cholesteryl esters in Leydig tumor cells.

Incubating MA-10 Leydig tumor cells with sodium oleate led to the accumulation of triglyceride within the cells. Triglycerides were deposited in a time- and dose-dependent fashion. Cellular triglyceride promoted storage of cholesteryl ester. As much cholesteryl ester was stored in oleate-treated cells as in cells treated with saturating concentrations of low density lipoprotein. Addition of both oleate and low density lipoprotein resulted in additive accumulation of cholesteryl esters. Cholesteryl esters in cells loaded with triglyceride by oleate treatment were mobilized in response to dibutyryl-cAMP to an extent similar to that in cells containing low triglyceride concentrations. Dibutyryl-cAMP stimulated cholesteryl ester mobilization under all conditions, and stimulated triglyceride mobilization when adequate fatty acid acceptors were available. The results indicate that while triglyceride accumulation in MA-10 cells promoted cholesteryl ester deposition, it did not impair cAMP-dependent cholesteryl ester hydrolysis or steroid hormone production.

Algestone↗
PubMed2004

Effects of dietary triglycerides on rheological properties of human red blood cells (abstract).

Atherogenic diets rich in saturated fat and cholesterol influence the blood viscosity and red blood cell (RBC) aggregability, the parameters associated with increased risk of circulatory disorders. However, little is known about the effect of triglycerides, which are the major dietary lipid form in humans, on blood rheology. Therefore, we studied the effects of postprandial plasma triglyceride levels on human RBC indices, hematological parameters, RBCs aggregation velocity and whole blood viscosity. For this purpose, whole blood was collected 2 hours after high-fat or low-fat meal. Proteins, triglycerides and cholesterol levels of plasma were analysed, and RBCs rouleaux formation rate was measured in 70% autologous plasma using a low-shear rheoscope. There were no significant differences in hematological parameters, RBC indices, whole blood viscosity, plasma protein and cholesterol content between high-fat and low-fat blood samples. However, a significant increase in rouleaux formation rate was observed in samples with high postprandial triglyceride levels, when compared with low-triglyceride samples. Plasma triglyceride levels correlated significantly with rouleaux formation rate. In conclusion, these results suggest that diet-dependent alterations of plasma triglyceride levels as well as possible changes in the cell membrane lipid composition lead to RBC hyperaggregability.

Adult↗
PubMed2004

Studies on serum triglyceride level in patients with myocardial infarction.

Myocardial Infarction (MI) is the most common form of heart disease and the single most important cause of premature death in the developed and developing world. Unfortunately the incidence of the condition is increasing rapidly in many developing countries like Bangladesh. Effort should therefore be taken to minimize the risk factors of MI. Large scale randomized clinical trials have shown that lowering high triglyceride concentration mainly by drugs reduces the risk of cardiac events like MI. So the present work has been designed to see the serum triglyceride levels in normal healthy subjects, to compare serum triglyceride levels in patients with MI and those of healthy subjects and to evaluate the association of serum triglyceride in Bangladeshi MI patients. The present study was carried out in the Department of Biochemistry, BSMMU in collaboration with Department of Cardiology, BSMMU and NICVD, Dhaka during the period of July 2001 to December 2002. A total of 50 subjects were selected, Group A (30 subjects of control ) and Group B (20 subjects of test ). The mean level of serum triglyceride in control subjects were 117.07 +/- 32.41 mg/d1 and in test subjects were 176.87 +/- 37.15 mg/d1. So the present study showed that serum triglyceride level is significantly higher in patients with MI. From the present study, it is difficult to draw any definite conclusion but suggested that high serum triglyceride concentration is a cause of the incidence of MI.

Adult↗
PubMed1992

Mechanisms of triglyceride-lowering effect of an HMG-CoA reductase inhibitor in a hypertriglyceridemic animal model, the Zucker obese rat.

Inhibitors of 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase have been approved for treatment of hypercholesterolemia in humans. This class of therapeutic agents, in addition to lowering plasma cholesterol, reduces plasma triglyceride levels. We have investigated the mechanism of triglyceride-lowering effect of lovastatin in the hypertriglyceridemic state by using a rodent model of hypertriglyceridemia and obesity, the Zucker obese (fa/fa) rat. Lovastatin treatment (4 mg/kg), as compared to placebo, caused a 338% reduction in plasma triglyceride (146 +/- 5 vs. 494 +/- 76 mg/dl), a 58% decrease in total cholesterol (99 +/- 13 vs. 156 +/- 18 mg/dl), and a 67% reduction in high density lipoprotein (HDL)-cholesterol (69 +/- 8 vs. 115 +/- 15 mg/dl). The fall seen in plasma triglyceride was due to a decrease in hepatic secretion of very low density lipoproteins (VLDL), determined after blocking the clearance of triglyceride-rich lipoproteins with Triton WR-1339. Lovastatin treatment did not affect either the activities of hepatic lipogenic enzymes, glucose-6-phosphate dehydrogenase, or malic enzyme, or the activities of the lipolytic enzymes of adipose tissue, lipoprotein lipase, or liver, hepatic triglyceride lipase. Supplementation of mevalonolactone in the diet partially reversed the changes in plasma triglyceride (265 +/- 37 vs. 146 +/- 5 mg/dl), but not in total or HDL-cholesterol. These data demonstrate that, in the hypertriglyceridemic Zucker rat model, HMG-CoA reductase inhibitors reduce the rate of secretion of VLDL and this effect can be partially reversed by administration of mevalonolactone.

Adipose Tissue↗
PubMed1975

Splanchnic and hepatic triglyceride secretion during hypercaloric intravenous glucose infusion in conscious swine.

We have validated a radiochemical technique for measuring the rate of secretion of plasma triglycerides from the liver and/or splanchnic region during the consumption of glucose under isotopic steady-state conditions. Values obtained with this technique correlated closely with those based on transhepatic or transsplanchnic chemical gradients (r = 0.95). Likewise, values for secretion of triglycerides obtained with the radiochemical technique correlated closely with those obtained for extrahepatic or extrasplanchnic triglyceride clearance. Values for mean net splanchnic and hepatic secretion of plasma triglyceride fatty acids, transported essentially in very low density lipoproteins, were 1.9 and 2.0 mumoles/min.kg body wt0.75, respectively, about one-half of the rate of transport of free fatty acids. However, the fraction of triglyceride fatty acids of plasma very low density lipoproteins that was derived from plasma free fatty acids averaged 9% and that derived from glucose, though increasing with time, reached only 2% after constant intravenous infusion of radioglucose for 5 hr. Porcine hepatic secretion of plasma triglycerides is large in the glucose-fed state, and the secreted triglyceride fatty acids evidently are derived from stored fat or glycon.

Abdomen↗
PubMed1975

Bivariate analyses of cholesterol and triglyceride levels in families in which probands have type IIb lipoprotein phenotype.

Univariate and bivariate analyses of cholesterol and triglycerides are performed after appropriate age adjustment on 247 individuals in 33 families where the probands have elevations of cholesterol, low density lipoprotein and triglycerides, and type IIb lipoprotein phenotype. Mixture of lognormal distributions are fitted by maximum likelihood to the data. Best fitting single and mixtures of lognormal distributions are compared with empirical cumulative plots, and the likelihood-ratio criterion is used to test for significance. A mixture of two lognormal distributions fits significantly better than one lognormal distribution for cholesterol but not for triglycerides. When a mixture of bivariate lognormals is fitted to the data, only one local maximum is found, suggesting action of a single genetic determinant in this sample. The best cutoff line is almost parallel to the triglyceride axis, indicating the relatively high involvement of cholesterol compared to triglycerides in separating the normal and abnormal groups. Using the best linear function, the difference in the two bivariate means is found to account for 61% of the total variation in log cholesterol and log triglycerides. To determine if the results are due to enrichment of the sample with familial hypercholesterolemia syndrome, seven families where the proband and/or any relative has tendon xanthomas are removed and the analyses repeated on the remaining 26 kindreds. The results of these analyses are virtually the same as those of the total sample. Also, a subsample of 21 families in which the proband and at least one additional kindred member are affected is analyzed in the same manner with similar results. For comparison, data from a study of families with combined hyperlipidemia [1] are analyzed in an analogous manner, bearing in mind that the populations sampled are probably different. Fitting a mixture of two bivariate distributions and finding the best cutoff to these data indicate that triglycerides are more involved in separating the two groups. Probably because of major differences in ascertainment, the distribution of lipid levels in oour patient group is practically indistinguishable from that of hypercholesterolemia, and the Seattle data [1] are more nearly similar to hypertriglyceridemia. It may be premature to consider familial combined hyperlipidemia as an entity distinct from both hypercholesterolemia and hypertriglyceridemia. We hope it will eventually be possible to analyze these data using a refined genetic model that includes both major gene and polygenic effects and to combine this form of analysis with quantitative tissue culture methods.

Adult↗
PubMed1991

Myocardial triglyceride turnover and contribution to energy substrate utilization in isolated working rat hearts.

The objective of this study was to determine the contribution of myocardial triglycerides to overall ATP production in isolated working rat hearts. Endogenous lipid pools were initially prelabeled (pulsed) by perfusing hearts for 60 min with Krebs-Henseleit buffer containing 1.2 mM [1-14C]palmitate. During a subsequent 60-min period (chase), hearts were perfused with either no fat, low fat (0.4 mM [9,10-3H] palmitate), or high fat (1.2 mM [9,10-3H]palmitate). All buffers contained 11 mM glucose. During the "chase," 14CO2 production (a measure of endogenous fatty acid oxidation) and 3H2O production (a measure of exogenous fatty acid oxidation) were determined. Oxidative rates of endogenous fatty acids during the chase were 279 +/- 50, 88 +/- 14, and 88 +/- 8 nmol of [14C]palmitate oxidized per g dry weight.min in the no fat, low fat, and high fat groups, respectively, compared to exogenous palmitate oxidation rates of 0, 361 +/- 68, and 633 +/- 60 nmol of [3H]palmitate/g dry weight.min, in the no fat, low fat, and high fat groups, respectively. Endogenous [14C]palmitate oxidation rates were matched by loss of [14C]palmitate from endogenous myocardial triglycerides. Overall triglyceride content decreased during the no fat and low fat chase perfusion but did not change during the high fat chase. Loss of triglyceride [14C]palmitate during the high fat chase was matched by incorporation of exogenous [3H]palmitate in triglycerides. In a second series of perfusions, three groups of hearts were perfused under similar conditions, except that unlabeled palmitate was used during the "pulse" and that 11 mM [2-3H/U-14C]glucose and unlabeled palmitate was present during the chase. During the chase, both glycolysis (3H2O production) and glucose oxidation (14CO2 production) rates were measured. Rates of glucose oxidation were inversely related to the fatty acid concentration in the perfusate (1257 +/- 158, 366 +/- 40, and 124 +/- 26 nmol of glucose oxidized per min.g dry weight in the no fat, low fat, and high fat groups, respectively), while rates of glycolysis were not significantly different between these groups. Calculation of overall ATP production from both oxidative and glycolytic sources determined that even in the presence of high concentrations of fatty acids, myocardial triglyceride turnover can provide over 11% of steady state ATP production in the aerobically perfused heart. In the absence of fatty acids, myocardial triglyceride fatty acids can become the major energy substrate of the heart.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1976

Maternal plasma triglycerides as a source of fetal fatty acids.

The transfer of plasma triglyceride fatty acids from mother to fetus was studied in rats. Following i.v. injection of labelled chylomicron and very low density lipoprotein (VLDL) triglycerides into the mother, the time courses of the plasma triglycerides, free fatty acids, and fetal radioactivity were determined. The data were analysed using a mathematical model. From the results the following conclusions were drawn: To cover the need of fetal fatty acids, the placenta utilizes only VLDL triglycerides but not chylomicron triglycerides. Comparison of the amount of VLDL triglyceride fatty acids (0.04 micromoles/min/litter) and of maternal plasma free fatty acids (0.08 micronmoles/min/litter) transferred into the fetus indicates that the maternal plasma triglycerides are a source of fetal fatty acids, that cannot be neglected.

Chylomicrons↗
PubMed1989

Comparison of the effects of enteral feeding with continuous and intermittent parenteral nutrition on hepatic triglyceride secretion in human beings.

Plasma triglyceride turnover was measured during steady-state conditions in 22 postoperative patients. Nine had received nutritional support with an enteral regimen, seven had received an equivalent regimen as continuous parenteral nutrition, and six received the same parenteral regimen as a cyclical infusion. After 5 days of nutritional support, each patient received an intravenous bolus of tritiated glycerol. Plasma radiolabeled triglyceride content was measured during the subsequent 24 hours. The data were analyzed by means of a simple deterministic model of plasma triglyceride kinetics and compared with the results obtained by stochastic analysis. The rates of hepatic triglyceride secretion obtained by deterministic analysis were higher than those obtained by the stochastic approach. However, the mode of delivery of the nutritional regimen did not affect the rate of hepatic triglyceride secretion regardless of the method of analysis. The results suggest that neither complete nutritional bypass of the gastrointestinal tract nor interruption of parenteral nutrition in an attempt to mimic normal eating has any effect on hepatic triglyceride secretion. Any beneficial effect that enteral feeding or cyclical parenteral nutrition may have on liver dysfunction associated with standard parenteral nutrition appears to be unrelated to changes in hepatic triglyceride secretion.

Aged↗
PubMed1988

Abdominal adipose tissue and serum HDL-cholesterol: association independent from obesity and serum triglyceride concentration.

It has been recently shown that an excess of abdominal fat was associated with reduced serum HDL-cholesterol level, supporting previous studies that have reported a relationship between fat distribution and cardiovascular risk factors. Since a negative relationship has been observed between serum triglyceride and HDL-cholesterol concentrations, the associations between body fat distribution and HDL-cholesterol level was studied with control over serum triglycerides in a sample of 429 healthy adult men. The relative distribution of subcutaneous fat, as reflected by the trunk to extremity skinfolds (T/E) ratio and the absolute amount of subcutaneous abdominal fat, obtained by the measurement of the abdominal skinfold thickness, were significantly correlated with serum triglycerides (r = 0.27 and 0.35 respectively, P less than 0.0001), with serum HDL-cholesterol (r = -0.14, P less than 0.01, and -0.26, P less than 0.0001) and with the serum HDL-cholesterol/total cholesterol ratio (r = -0.25 and -0.39, P less than 0.0001). Analysis of variance on two factors, the T/E ratio and the body mass index (BMI), revealed significant and independent effects of adiposity and relative distribution of subcutaneous fat on serum lipids and HDL-cholesterol (0.05 greater than P less than 0.001). However, when comparable analyses of variance were performed to study the respective contributions of obesity (as measured by the BMI) and the absolute amount of abdominal fat (as measured by the abdominal skinfold), most of the variance in serum triglycerides, cholesterol and HDL-cholesterol was explained by abdominal fat alone and not by the BMI. Therefore, it appeared that with the exception of the HDL-cholesterol/total cholesterol ratio, the association between obesity and serum lipids and HDL-cholesterol was, in the present sample, primarily explained by the amount of abdominal fat. As reported by others, serum triglyceride level was negatively correlated with HDL-cholesterol (r = -0.33, P less than 0.0001) and the HDL-cholesterol/total cholesterol ratio (r = -0.54, P less than 0.0001). After cholesterol and HDL-cholesterol scores were adjusted for the effect of triglycerides, the T/E ratio was no longer associated with serum HDL-cholesterol whereas the abdominal skinfold remained significantly correlated with serum HDL-cholesterol concentration (r = -0.16, P less than 0.01). These results suggest that a portion of the association between body fat topography and serum HDL-cholesterol is mediated by the effect of fat distribution on serum triglycerides.(ABSTRACT TRUNCATED AT 400 WORDS)

Abdominal Muscles↗
PubMed1987

[Triglyceride fatty acids of abdominal adipose tissue in two lines of chickens rendered lean or fat by selection].

Newly-hatched chickens from two lines selected for high or low abdominal fat/live weight ratio, were fed on a stock low-lipid diet (2.9 wt % lipids) for nine weeks. Linoleic acid made up 54.3% of dietary fatty acids. Their abdominal adipose tissue and liver triglycerides were then isolated for fatty acid analysis. The linoleic acid content of abdominal fat triglycerides was higher in lean than in fat chickens (19.2 vs 16.4% of triglyceride fatty acids, respectively). This difference was highly significant. Conversely, the level of monounsaturated fatty acids in the abdominal fat triglycerides was significantly lower (especially palmitoleic acid) in lean than in fat chickens. The proportion of linoleic acid in liver triglycerides was also higher in lean than in fat chickens (12.2 vs 5.5% of triglyceride fatty acids). The higher dilution of dietary linoleic acid within the depot fat of the fat line chickens shows that the flux of endogenous fatty acids from the liver was larger in these animals than in the lean ones. Moreover, the elevated amounts of palmitoleic acid (virtually absent from the diet) in the depot and liver triglycerides of fat chickens, was most likely caused by a higher delta 9-desaturating activity in the liver of the latter animals.

Abdomen↗
PubMed1985

Contributions of fatty acid and sterol synthesis to triglyceride and cholesterol secretion by the perfused rat liver in genetic hyperlipemia and obesity.

The relative importance of fatty acid synthesis in triglyceride secretion by perfused livers from lean (normal control) and obese Zucker rats was investigated. Livers from fed animals were perfused in a recirculating system with tritiated water and a constant infusion of oleic acid. Triglyceride secretion was 5 times greater and cholesterol secretion was 35% greater in the obese rat livers. The very-low-density lipoprotein hypersecreted by perfused livers from obese rats contained more apolipoprotein B and exhibited an increased B-48/B-100 ratio. Apo-B was also elevated in the hypertriglyceridemic plasma of obese rats in both fed and fasting states. The very-low-density lipoprotein isolated therefrom was likewise characterized by an increased B-48/B-100 ratio. Ketogenesis was depressed 40% in the obese rat livers and increased hepatic malonyl-CoA was implicated in this alteration. The de novo synthesis and secretion of newly synthesized cholesterol was moderately increased in the perfused livers from obese rats. Tritium incorporation into fatty acids was 15 times greater in the obese genotype. Most of the synthesized fatty acids remained in the liver and were recovered after perfusion in triglyceride and phospholipids. Newly synthesized fatty acids accounted for only 3 and 15% of the triglyceride secreted by the lean and obese rat livers, respectively. A large portion of the secreted triglyceride fatty acids was derived from endogenous liver lipids. When the turnover of newly synthesized fatty acids in these pools was considered, the contribution of de novo fatty acid synthesis to triglyceride secretion was estimated to be 9% in the lean and 44% in the obese rat livers. Therefore, the altered partition of free fatty acids (Fukuda, N., Azain, M. J., and Ontko, J. A. (1982) J. Biol. Chem. 257, 14066-14072) and increased fatty acid synthesis are both major determinants of the hypersecretion of triglyceride-rich lipoproteins by the liver in the genetically obese Zucker rat.

Animals↗
PubMed1985

Effects of medium-chain triglyceride feeding or glucose infusion on glucose kinetics in the newborn rat.

Hypoglycaemia which develops in starved newborn rats (0.15 +/- 0.01 mg/ml) is reversed by feeding medium-chain triglycerides (0.66 +/- 0.05 mg/ml). Despite similar glycaemia (0.71 +/- 0.07 mg/ml) starved newborns infused with glucose (10.7 mg/min/kg) show a 30% higher glucose turnover rate than medium-chain triglyceride fed animals (14.1 +/- 0.6 versus 10.6 +/- 0.3 mg/min/kg, p less than 0.01). For a comparable [6-3H]glucose turnover rate (10.5 +/- 0.3 mg/min/kg), glucose-infused (5.25 mg/min/kg) newborns have a 30% lower glycaemia (0.50 +/- 0.03 mg/ml, p less than 0.01) than medium-chain triglyceride-fed newborns. Thus, medium chain triglyceride feeding leads to a 30% decreased capacity of the tissues to utilize glucose. For a similar glucose turnover rate, medium-chain triglyceride-fed newborns have a higher blood lactate concentration than glucose-infused newborns (0.26 +/- 0.03 versus 0.15 +/- 0.02 mg/ml). However, in medium-chain triglyceride-fed newborns, the increase of blood lactate is not only due to the Cori cycle, as glucose recycling is less increased than glucose production. Thus medium-chain triglyceride increases the release of gluconeogenic precursors which are not derived from blood glucose. In presence of a glucose infusion (15.25 mg/min/kg) producing hyperglycaemia (1.35 +/- 0.05 mg/ml), endogenous glucose production is suppressed by only 37%. If 3-mercaptopicolinate, an inhibitor or gluconeogenesis, is given concomitantly, hyperglycaemia is prevented (0.72 +/- 0.08 mg/ml) and endogenous glucose production is suppressed. Glucose infusion in the hypoglycaemic newborn rat might thus lead to a precarious glucose homeostasis.

Animals↗